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Apoptosis signal-regulating kinase-1 aggravates ROS-mediated striatal

Title
 Apoptosis signal-regulating kinase-1 aggravates ROS-mediated striatal 
Authors
 Kyoung Joo Cho ; Hyun Woo Kim ; Gyung Whan Kim ; Jong Eun Lee ; So Yeong Cheon 
Issue Date
2013
Journal Title
 Biochemical and Biophysical Research Communications 
ISSN
 0006-291X 
Citation
 Biochemical and Biophysical Research Communications, Vol.441(2) : 280~285, 2013 
Abstract
Apoptosis signal-regulating kinase-1 (ASK1), an early signaling element in the cell death pathway, has been suggested to participate in the pathology of neurodegenerative diseases, which may be associated with environmental factors that impact the diseases. Although it is not entirely elucidated, 3-nitropropionic acid (3-NP) provokes mitochondrial dysfunction and selectively forms striatal lesions similar to those found in Huntington’s disease. The current study investigated whether ASK1 is involved in striatal pathology following chronic systemic infusion of 3-NP. The results show that ASK1 acts as a primary mediator of there active oxygen species (ROS) cell death signal cascade in the 3-NP-damaged striatal region by disrupting the positive feedback cycle. In 3-NP-infused striatal lesions, ROS increased ASK1. Superoxide dismutase transgenic (SOD-tg) mice reduced ASK1by scavenging ROS, and reduction of ASK1leads to a reduction in cell death. However, ASK1 down-regulation in 3-NP infusion mice also decreased striatal cell death without scavenging ROS. In contrast decreasing cell death by si-ASK1 treatment along with 3-NP in both SOD tg and wild-type mice (wt), cell death rebounded when ASK1 peptide was added to SOD tg mice. The present study suggests that ROS-inducing ASK1 may be an important step in the pathogenesis of 3-NP infused striatal lesions in murine brains.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/88490
DOI
10.1016/j.bbrc.2013.08.103
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Anatomy
1. 연구논문 > 1. College of Medicine > Dept. of Neurology
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
Yonsei Authors
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Link
 http://www.sciencedirect.com/science/article/pii/S0006291X13014769
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